Chronic stress at work and the metabolic syndrome: prospective study

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there appears to be a positve correlation between metabolic syndrome
and the incidence of chronic stress among secondary school teachers.this
may be particularly true among teachers working with high risk students.my
opinion.

Chandola and colleagues present data from the Whitehall II Study correlating the relationship between self-reported stress and the metabolic syndrome. The paper does not comment on the "elephant in the room" that is the relationship between self-reported stress and "objective" measures of psychosocial adversity. The notion of an objective measure of such adversity may be an oxymoron but surely this is a key consideration if this study, which is essentially ecological, is not to be misrepresented.

Chandola and colleagues state in their discussion that "greater exposure to job stress over 14 years was linked to greater risk of metabolic syndrome in a dose-response manner." What the study does perhaps demonstrate is the way in which self-reported work stress clusters with a range of non-adaptive coping responses such as excess alcohol consumption and failure to engage in self care behaviours such as exercise. Stress is a complex personal construct and not the unproblematic external variable which Chandola et. al. might suggest they have measured.

Chandola and colleagues (1) have amassed an intriguing dataset to
permit hypotheses to be generated around the relationships between
occupational grade, work stress and cardiovascular disease. They have,
however, fallen into the trap of confusing a clinical clustering of risk
factors, the Metabolic Syndrome, with a physiological construct.

The associations between dyslipidaemia, hypertension, glucose
intolerance and central obesity have been recognised for decades. In
1988, Reaven proposed insulin resistance as an underlying mechanism for
this clustering, which he termed Syndrome X (2). However he excluded
obesity from the component parts of this Syndrome because, as he has
recently pointed out (3), it is not a consequence of insulin resistance,
but only increases its likelihood. The definition of Metabolic Syndrome
employed by Chandola et al is that of the NCEP-ATP III (4), a Panel
concerned with clinical identification of subjects at high cardiovascular
risk. The Panel report notes that excess body fat (particularly abdominal
obesity) and physical inactivity are important determinants of the
cluster, and major targets of treatment. There is, then, a danger of
confusing aetiology with outcome by the inclusion of abdominal obesity as
one of the three risk factors used to define the presence of the Metabolic
Syndrome.

Previous studies from Brunner, Marmot and colleagues, based on this
same Whitehall II cohort, have shown cross-sectional relationships between
employment grade and central obesity (5), and longitudinal relationships
between work stress and weight gain over a five year follow-up (6). It
seems likely, then, that at least some of the work stress-Metabolic
Syndrome relationship in the current study is simply the consequence of
greater weight gain in people subject to chronic work stress.

The Whitehall II study nevertheless provides a potentially valuable
resource for a more rigorous exploration of mechanisms. The dominant
paradigm to explain the Metabolic Syndrome is that of low-grade
inflammation (7), consequent upon generation of adipocytokines,
particularly from visceral fat (8), which may also account for both
insulin resistance and vascular disease (9). While longitudinal changes
in body-mass index are likely to represent the consequences of positive
energy balance (greater calorie intake or reduced physical activity), the
relationship between employment grade or work stress and central
distribution of fat is more intriguing. Thus, while in part this may be
consequent upon differences in physical activity or in smoking, the
potential role of the hypothalamo-pituitary-adrenal (HPA) axis is worth
exploring. More sophisticated modelling might permit testing the role of
adipose tissue-generated cytokines in activating this HPA axis (10), and
in the autonomic nervous system changes which this group has also linked
to the Metabolic Syndrome (11). However, any independent relationship of
employment grade or work stress with components of the Metabolic Syndrome
other than obesity will require rigorous adjustment for the confounding
influence of body fat mass.

4. Expert Panel on Detection, Evaluation and Treatment of High Blood
Cholesterol in Adults (Adult Treatment Panel III). Executive Summary of
the Third Report of the National Cholesterol Education Program (NCEP).
JAMA 2001; 285: 2486-2497.

The major sequelae of metabolic syndrome, also known as syndrome X
are cardiovascular disease and type 2 diabetes mellitus, but the syndrome
also increases the risk of polycystic ovary syndrome, fatty liver,
cholesterol gallstones, asthma, sleep disturbances, and some forms of
cancer.Nuclear receptors are transcription factors that serve as
intracellular receptors for endocrine hormones and dietary lipids.The
retinoid X receptor (RXR), a member of the nuclear-receptor superfamily,
is a common binding partner for a subgroup of other nuclear receptors. The
resulting functional complex of one RXR molecule with one distinct nuclear
-receptor molecule is known as a heterodimer. Drugs that target RXR and
its heterodimerization partners are are important in clinical use for the
treatment of cancer, dermatologic diseases, endocrine disorders, and the
metabolic syndrome.
Reference:
Shulman AI, Mangelsdorf DJ. Retinoid X receptor heterodimers in the
metabolic syndrome. N Engl J Med 2005;353:604-615.

The prospective study by Chandola et al [1] adds a further Public
Health imperative to reduce the significant morbidity, consequent on
chronic stress at work. This week a BUPA Insurance survey [2] found seven
million Britons feel so ill with 'worry' that they seek medical help. In
the employed population, the British Occupational Health Research
Foundation found 'the largest, and growing, cause of work-related ill
health' is now mental ill health [3]. They have looked at a number of
remedial interventions, generally at the level of individual sick
employees, such as cognitive behavioural therapy. In terms of the social
gradient of illness described among civil servants [1], individual
interventions worked best 'with employees in high-control jobs' [3].
Employers have a legal 'duty of care' to protect the health of all their
employees, and the Health and Safety Executive have published Management
Standards aiming to reduce 'stress at work' [4]. In terms of reducing
chronic stress, it may help to consider change at the level of positive
'wellness' for the whole organisation, perhaps using a 'social engagement'
model [5] with dynamic learning-in-action.

metabolic syndrome also called X syndrome is caused by insulin
resistence and beside stress there are number of other causes of this
syndrome.being overweight,eating lot of carbohydrate rich food like
pasta,bread,rice,potatoes
and refined sugars,they all disturb the balance between glucose and
insulin.sedantary life style ie not doing excercise is also another risk
factor and there is also genetic predisposition to metabolic syndrome.